Bell’s palsy

DEFINISI

Bell’s palsy merupakan paresis nervus fasialis perifer yang

penyebabnya tidak diketahui (idiopatik) dan bersifat akut. Banyak

yang mencampuradukkan antara Bell’s palsy dengan paresis

nervus fasialis perifer lainnya yang penyebabnya diketahui.

Biasanya penderita mengetahui kelumpuhan fasialis dari teman

atau keluarga atau pada saat bercermin atau sikat gigi/berkumur.

Pada saat penderita menyadari bahwa ia mengalami kelumpuhan

pada wajahnya, maka ia mulai merasa takut, malu, rendah diri,

mengganggu kosmetik dan kadangkala jiwanya tertekan terutama

pada wanita dan pada penderita yang mempunyai profesi yang

mengharuskan ia untuk tampil di muka umum. Seringkali timbul

pertanyaan didalam hatinya, apakah wajahnya bisa kembali secara

normal atau tidak.

Bell’s palsy adalah kelumpuhan fasialis perifer yang belum

diketahui penyebabnya, bisa akibat proses non-supuratif, non-

neoplasmatik, non-degeneratif primer namun sangat mungkin

akibat edema jinak pada bagian nervus fasialis di foramen

stilomastoideus atau sedikit proksimal dari foramen tersebut, yang

mulanya akut dan dapat sembuh sendiri tanpa pengobatan.

B. EPIDEMIOLOGI

Di Indonesia, insiden Bell’s palsy secara pasti sulit ditentukan.

Data yang dikumpulkan dari 4 buah Rumah sakit di Indonesia

didapatkan frekuensi Bell’s palsy sebesar 19,55 % dari seluruh

kasus neuropati dan terbanyak pada usia 21 – 30 tahun. Lebih

sering terjadi pada wanita daripada pria. Tidak didapati perbedaan

insiden antara iklim panas maupun dingin, tetapi pada beberapa

penderita didapatkan adanya riwayat terpapar udara dingin atau

angin berlebihan.

C. ETIOLOGI

Banyak kontroversi mengenai etiologi dari Bell’s palsy, tetapi ada

4 teori yang dihubungkan dengan etiologi Bell’s palsy yaitu :

1. Teori Iskemik vaskuler

Nervus fasialis dapat menjadi lumpuh secara tidak langsung karena

gangguan regulasi sirkulasi darah di kanalis fasialis.

2. Teori infeksi virus

Virus yang dianggap paling banyak bertanggungjawab adalah

Herpes Simplex Virus (HSV), yang terjadi karena proses reaktivasi

dari HSV (khususnya tipe 1).

3. Teori herediter

Bell’s palsy terjadi mungkin karena kanalis fasialis yang sempit

pada keturunan atau keluarga tersebut, sehingga menyebabkan

predisposisi untuk terjadinya paresis fasialis.

4. Teori imunologi

Dikatakan bahwa Bell’s palsy terjadi akibat reaksi imunologi

terhadap infeksi virus yang timbul sebelumnya atau sebelum

pemberian imunisasi.

D. PATOFISIOLOGI

Apapun sebagai etiologi Bell’s palsy, proses akhir yang dianggap

bertanggungjawab atas gejala klinik Bell’s palsy adalah proses

edema yang selanjutnya menyebabkan kompresi nervus fasialis.

Gangguan atau kerusakan pertama adalah endotelium dari kapiler

menjadi edema dan permeabilitas kapiler meningkat, sehingga

dapat terjadi kebocoran kapiler kemudian terjadi edema pada

jaringan sekitarnya dan akan terjadi gangguan aliran darah

sehingga terjadi hipoksia dan asidosis yang mengakibatkan

kematian sel. Kerusakan sel ini mengakibatkan hadirnya enzim

proteolitik, terbentuknya peptida-peptida toksik dan pengaktifan

kinin dan kallikrein sebagai hancurnya nukleus dan lisosom. Jika

dibiarkan dapat terjadi kerusakan jaringan yang permanen.

E. GAMBARAN KLINIS

Biasanya timbul secara mendadak, penderita menyadari adanya

kelumpuhan pada salah satu sisi wajahnya pada waktu bangun

pagi, bercermin atau saat sikat gig/berkumur atau diberitahukan

oleh orang lain/keluarga bahwa salah satu sudutnya lebih rendah.

Bell’s palsy hampir selalu unilateral. Gambaran klinis dapat berupa

hilangnya semua gerakan volunter pada kelumpuhan total. Pada

sisi wajah yang terkena, ekspresi akan menghilang sehingga

lipatan nasolabialis akan menghilang, sudut mulut menurun, bila

minum atau berkumur air menetes dari sudut ini, kelopak mata

tidak dapat dipejamkan sehingga fisura papebra melebar serta kerut

dahi menghilang. Bila penderita disuruh untuk memejamkan

matanya maka kelopak mata pada sisi yang lumpuh akan tetap

terbuka (disebut lagoftalmus) dan bola mata berputar ke atas.

Keadaan ini dikenal dengan tanda dari Bell (lagoftalmus disertai

dorsorotasi bola mata). Karena kedipan mata yang berkurang maka

akan terjadi iritasi oleh debu dan angin, sehingga menimbulkan

epifora.1,6 Dalam mengembungkan pipi terlihat bahwa pada sisi

yang lumpuh tidak mengembung.6 Disamping itu makanan

cenderung terkumpul diantara pipi dan gusi sisi yang lumpuh.1

Selain kelumpuhan seluruh otot wajah sesisi, tidak didapati

gangguan lain yang mengiringnya, bila paresisnya benar-benar

bersifat “Bell’s palsy”.

F. DIAGNOSIS

Diagnosa ditegakkan berdasarkan anamnesa serta beberapa

pemeriksaan fisik, dalam hal ini yaitu pemeriksaan neurologis.

1. Anamnesa :

- Rasa nyeri.

- Gangguan atau kehilangan pengecapan.

- Riwayat pekerjaan dan adakah aktivitas yang dilakukan pada

malam hari di ruangan terbuka atau di luar ruangan.

- Riwayat penyakit yang pernah dialami oleh penderita seperti

infeksi saluran pernafasan, otitis, herpes, dan lain-lain.

2. Pemeriksaan :

- Pemeriksaan neurologis ditemukan paresis N.VII tipe

perifer.

- Gerakan volunter yang diperiksa, dianjurkan minimal :

1. Mengerutkan dahi

2. Memejamkan mata

3. Mengembangkan cuping hidung

4. Tersenyum

5. Bersiul

6. Mengencangkan kedua bibir

Untuk mengevaluasi kemajuan motorik penderita Bell’s palsy

memakai SKALA UGO FISCH

SKALA UGO FISCH

Dinilai kondisi simetris atau asimetris antara sisi sehat dan sisi

sakit pada 5 posisi :

Posisi Nilai Persentase (%)

0, 30, 70, 100

Skor

Istirahat 20

Mengerutkan dahi 10

Menutup mata 30

Tersenyum 30

Bersiul 10

Total

Penilaian persentase :

- 0 % : asimetris komplit, tidak ada gerakan volunter

- 30 % : simetris, poor/jelek, kesembuhan yang ada lebih dekat ke

asimetris komplit daripada simetris normal.

- 70 % : simetris, fair/cukup, kesembuhan parsial yang

cenderung ke arah normal

- 100% : simetris, normal/komplit

3. Diagnosa Klinis : Ditegakkan dengan adanya paresis N.VII

perifer dan bukan sentral. Umumnya unilateral

4. Diagnosa Topik :

Letak Lesi

Kelain

an

motori

k

Gangguan

pengecap

an

Gangguan

pendengaran

Hiposekre

si saliva

Hiposekre

si

lakrimalis

Pons-meatus

akustikus

internus

+ +

+

tuli/hiperaku

sis

+ +

Meatus

akustikus

internus-

ganglion

genikulatum

+ + +

Hiperakusis + +

Ganglion

genikulatum-

N. Stapedius

+ + +

Hiperakusis + -

N.stapedius-

chorda

tympani

+ + + + -

Chorda

tympani + + - + -

Infra chorda

tympani-

sekitar

foramen

stilomastoideu

s

+ - - - -

5. Diagnosa etiologi : Sampai saat ini etiologi Bell’s palsy yang

jelas tidak diketahui.

6. Diagnosa banding :

1. Otitis Media Supurativa dan Mastoiditis

2. Herpes Zoster Oticus

3. Trauma kapitis

4. Sindroma Guillain – Barre

5. Miastenia Gravis

6. Tumor Intrakranialis

G. PROGNOSIS

Sembuh spontan pada 75-90 % dalam beberapa minggu atau dalam

1-2 bulan. Kira-kira 10-15 % sisanya akan memberikan gambaran

kerusakan yang permanen.

H. KOMPLIKASI

1. Crocodile tear phenomenon Yaitu keluarnya air mata pada saat

penderita makan makanan. Ini timbul beberapa bulan setelah

terjadi paresis dan terjadinya akibat dari regenerasi yang salah dari

serabut otonom yang seharusnya ke kelenjar saliva tetapi menuju

ke kelenjar lakrimalis. Lokasi lesi di sekitar ganglion

genikulatum.1

2. Synkinesis. Dalam hal ini otot-otot tidak dapat digerakkan satu

per satu atau tersendiri; selalu timbul gerakan bersama. Misal bila

pasien disuruh memejamkan mata, maka akan timbul gerakan

(involunter) elevasi sudut mulut, kontraksi platisma, atau

berkerutnya dahi. Penyebabnya adalah innervasi yang salah,

serabut saraf yang mengalami regenerasi bersambung dengan

serabut-serabut otot yang salah.

3. Hemifacial spasm. Timbul “kedutan” pada wajah (otot wajah

bergerak secara spontan dan tidak terkendali) dan juga spasme otot

wajah, biasanya ringan. Pada stadium awal hanya mengenai satu

sisi wajah saja, tetapi kemudian dapat mengenai pada sisi lainnya.

Kelelahan dan kelainan psikis dapat memperberat spasme ini.

Komplikasi ini terjadi bila penyembuhan tidak sempurna, yang

timbul dalam beberapa bulan atau 1-2 tahun kemudian.

4. Kontraktur. Hal ini dapat terlihat dari tertariknya otot, sehingga

lipatan nasolabialis lebih jelas terlihat pada sisi yang lumpuh

dibanding pada sisi yang sehat. Terjadi bila kembalinya fungsi

sangat lambat. Kontraktur tidak tampak pada waktu otot wajah

istirahat, tetapi menjadi jelas saat otot wajah bergerak.

I. TERAPI

a) Terapi medikamentosa : Golongan kortikosteroid sampai

sekarang masih kontroversi, Juga dapat diberikan neurotropik.

b) Terapi operatif : Tindakan bedah dekompresi

masih kontroversi

c) Rehabilitasi Medik

Rehabilitasi medik menurut WHO adalah semua tindakan yang

ditujukan guna mengurangi dampak cacat dan handicap serta

meningkatkan kemampuan penyandang cacat mencapai integritas

sosial.

Tujuan rehabilitasi medik adalah :

1. Meniadakan keadaan cacat bila mungkin

2. Mengurangi keadaan cacat sebanyak mungkin

3. Melatih orang dengan sisa keadaan cacat badan untuk dapat

hidup dan bekerja dengan apa yang tertinggal.

Untuk mencapai keberhasilan dalam tujuan rehabilitasi yang

efektif dan efisien maka diperlukan tim rehabilitasi medik yang

terdiri dari dokter, fisioterapis, okupasi terapis, ortotis prostetis,

ahli wicara, psikolog, petugas sosial medik dan perawat rehabilitasi

medik.

Sesuai dengan konsep rehabilitasi medik yaitu usaha gabungan

terpadu dari segi medik, sosial dan kekaryaan, maka tujuan

rehabilitasi medik pada Bell’s palsy adalah untuk

mengurangi/mencegah paresis menjadi bertambah dan membantu

mengatasi problem sosial serta psikologinya agar penderita tetap

dapat melaksanakan aktivitas kegiatan sehari-hari. Program-

program yang diberikan adalah program fisioterapi, okupasi terapi,

sosial medik, psikologi dan ortotik prostetik, sedang program

perawat rehabilitasi dan terapi wicara tidak banyak berperan.

Program Fisioterapi

- Pemanasan

1. Pemanasan superfisial dengan infra red.

2. Pemanasan dalam berupa Shortwave Diathermy atau

Microwave Diathermy

- Stimulasi listrik

Tujuan pemberian stimulasi listrik yaitu menstimulasi otot untuk

mencegah/memperlambat terjadi atrofi sambil menunggu proses

regenerasi dan memperkuat otot yang masih lemah. Misalnya

dengan faradisasi yang tujuannya adalah untuk menstimulasi otot,

reedukasi dari aksi otot, melatih fungsi otot baru, meningkatkan

sirkulasi serta mencegah/meregangkan perlengketan. Diberikan 2

minggu setelah onset.

- Latihan otot-otot wajah dan massage wajah

Latihan gerak volunter otot wajah diberikan setelah fase akut.

Latihan berupa mengangkat alis tahan 5 detik, mengerutkan dahi,

menutup mata dan mengangkat sudut mulut, tersenyum,

bersiul/meniup (dilakukan didepan kaca dengan konsentrasi

penuh).

Massage adalah manipulasi sitemik dan ilmiah dari jaringan tubuh

dengan maksud untuk perbaikan/pemulihan. Pada fase akut, Bell’s

palsy diberi gentle massage secara perlahan dan berirama. Gentle

massage memberikan efek mengurangi edema, memberikan

relaksasi otot dan mempertahankan tonus otot.1,3 Setelah lewat fase

akut diberi Deep Kneading Massage sebelum latihan gerak

volunter otot wajah. Deep Kneading Massage memberikan efek

mekanik terhadap pembuluh darah vena dan limfe, melancarkan

pembuangan sisa metabolik, asam laktat, mengurangi edema,

meningkatkan nutrisi serabut-serabut otot dan meningkatkan

gerakan intramuskuler sehingga melepaskan perlengketan.11

Massage daerah wajah dibagi 4 area yaitu dagu, mulut, hidung dan

dahi. Semua gerakan diarahkan keatas, lamanya 5-10 menit.

Program Terapi Okupasi

Pada dasarnya terapi disini memberikan latihan gerak pada otot

wajah. Latihan diberikan dalam bentuk aktivitas sehari-hari atau

dalam bentuk permainan. Perlu diingat bahwa latihan secara

bertahap dan melihat kondisi penderita, jangan sampai melelahkan

penderita. Latihan dapat berupa latihan berkumur, latihan minum

dengan menggunakan sedotan, latihan meniup lilin, latihan

menutup mata dan mengerutkan dahi di depan cermin.

Program Sosial Medik

Penderita Bell’s palsy sering merasa malu dan menarik diri dari

pergaulan sosial. Problem sosial biasanya berhubungan dengan

tempat kerja dan biaya. Petugas sosial medik dapat membantu

mengatasi dengan menghubungi tempat kerja, mungkin untuk

sementara waktu dapat bekerja pada bagian yang tidak banyak

berhubungan dengan umum. Untuk masalah biaya, dibantu dengan

mencarikan fasilitas kesehatan di tempat kerja atau melalui

keluarga. Selain itu memberikan penyuluhan bahwa kerja sama

penderita dengan petugas yang merawat sangat penting untuk

kesembuhan penderita.

Program Psikologik

Untuk kasus-kasus tertentu dimana ada gangguan psikis amat

menonjol, rasa cemas sering menyertai penderita terutama pada

penderita muda, wanita atau penderita yang mempunyai profesi

yang mengharuskan ia sering tampil di depan umum, maka

bantuan seorang psikolog sangat diperlukan.

Program Ortotik – Prostetik

Dapat dilakukan pemasangan “Y” plester dengan tujuan agar sudut

mulut yang sakit tidak jatuh. Dianjurkan agar plester diganti tiap 8

jam. Perlu diperhatikan reaksi intoleransi kulit yang sering terjadi.

Pemasangan “Y” plester dilakukan jika dalam waktu 3 bulan

belum ada perubahan pada penderita setelah menjalani fisioterapi.

Hal ini dilakukan untuk mencegah teregangnya otot Zygomaticus

selama parese dan mencegah terjadinya kontraktur.

Home Program :

1. Kompres hangat daerah sisi wajah yang sakit selama 20 menit

2. Massage wajah yang sakit ke arah atas dengan menggunakan

tangan dari sisi wajah yang sehat

3. Latihan tiup lilin, berkumur, makan dengan mengunyah disisi

yang sakit, minum dengan sedotan, mengunyah permen karet

4. Perawatan mata :

1. Beri obat tetes mata (golongan artifial tears) 3x sehari

2. Memakai kacamata gelap sewaktu bepergian siang hari, dan

Biasakan menutup kelopak mata secara pasif sebelum tidur.

Bell's Palsy During Pregnancy

For reasons not completely understood, women may develop Bell's palsy during pregnancy more frequently than the general population. The risk of Bell's palsy during pregnancy is thought to be greatest during the third trimester, or within several weeks of delivery. The prognosis for women with Bell's palsy during pregnancy is generally good. Bell's palsy does not appear to have any effect on the growing fetus.

Bell's Palsy During Pregnancy: A Summary Bell's palsy is a form of temporary facial paralysis resulting

from damage or trauma to a facial nerve. Because of this damage, people with Bell's palsy experience symptoms that can

include:

• Twitching, weakness, or paralysis of on one or both sides of the

face

• Drooping eyelid or corner of the mouth

• Drooling

• Dry eye or mouth

• Impairment of taste

• Excessive tearing in the eye.

•

For reasons not completely understood, women who are pregnant develop Bell's palsy more frequently than the general

population. The risk of Bell's palsy during pregnancy is thought to

be greatest during the third trimester, or within several weeks of delivery.

Bell's Palsy During Pregnancy: Treatment and Prognosis For women who develop Bell's palsy during pregnancy, treatment

is supportive, meaning that the symptoms, such as pain, are treated. Steroids and antiviral medicines are not recommended

for pregnant women.

The prognosis for women with Bell's palsy during pregnancy is

generally good. The extent of nerve damage determines the extent of Bell's palsy recovery time. Generally, improvement

of Bell's palsy is gradual but recovery times vary. The complete

recovery time for most women who develop Bell's palsy during pregnancy is six months or less.

For some women, however, the Bell's palsy recovery time may be longer or the symptoms may never completely disappear. This

is especially true for women who develop complete facial

paralysis as a result of Bell's palsy during pregnancy. In one study, only about half of the women with complete facial

paralysis that developed Bell's palsy during pregnancy recovered

to a satisfactory level.

Bell's palsy does not appear to have any effect on the growing

fetus. Women who develop Bell's palsy during pregnancy are also at

increased risk for developing preeclampsia. Because of this

increased risk, a woman who develops Bell's palsy during pregnancy will be monitored more closely for increases in blood

pressure and preeclampsia.

BELL’S PALSY (Syaraf) Dibuat oleh: Hariadi Supanto,Modifikasi terakhir pada Sat 29 of May, 2010 [04:52

UTC]

PRESENTASI KASUS PASIEN POLIKLINIK

REHABILITASI MEDIK

BELL’S PALSY

Anamnesis : Autoanamnesis

No. CM : 110856

Jam : 08.45 WIB

Ruang : Poliklinik Rehabilitasi Medik

I. IDENTITAS PASIEN

Nama : Tn. A

Umur : 43 tahun

Jenis Kelamin : Laki-laki

Alamat : Kauman, Mangunsari, Salatiga

Pekerjaan : PNS

Agama : Islam

II. DATA SUBYEKTIF

Keluhan Utama : Mulut perot ke kanan dan muka sebelah kiri terasa

tebal.

Kronologis : Pasien datang dengan keluhan mulut perot

kekanan dan muka sebelah kiri terasa tebal setelah bangun tidur pada pagi hari.

Pasien baru menyadarinya setelah ber wudlu mau sholat Subuh waktu

menyemburkan air wudlu melalui mulut air wudlu menyembur keluar melalui sudut

mulut sebelah kiri. 2 hari sebelumnya pasien merasakan sakit kepala dan pada

malam harinya pasien minum obat Oskadon selama 2 malam. Disamping itu pasien

juga merasakan bicaranya terganggu (cedal-cedal) dan tidak bisa menutup kelopak

mata sebelah kiri. Pasien kemudian berobat ke Puskesmas dan oleh dokter di

Puskesmas disarankan periksa ke bagian saraf. Setelah periksa ke bagian saraf BP

RSUD Salatiga pasien kemudian dirujuk kebagian Rehabilitasi Medik BP RSUD

WIROSABAN.

Faktor yang memperberat : -

Faktor yang memperingan : -

Gejala penyerta : -

Riwayat Penyakit Dahulu : Hipertensi (+) hiperkolestrolemia (+), DM (-) trauma

(-), Jantung (-)

Riwayat Penyakit Keluarga : Tidak ada anggota keluarga yang menderita

penyakit serupa.

Riwayat sosial ekonomi : Pasien adalah seorang Pegawai Negeri Sipil dengan

gaji rata-rata Rp. 2.000.000,00/bulan

III. DATA OBYEKTIF

A. Status present

Tekanan darah : 120/80 mmHg

Denyut nadi : 72 x/menit

Pernafasan : 20 x/menit

Suhu : 36,40C

B. Status Internus

Kepala : Mesosepal, bentuk simetris.

Leher : Pembesaran kelenjar limfe (-), kaku kuduk (-),

bentuk vertebra normal, nyeri tekan vertebra (-).

Dada : Jantung dan Paru dalam batas normal

Abdomen : Hepar dan lien dalam batas normal.

C. Status Psikis

Dalam batas normal

D. Status Neurologis

Kesadaran : Compos Mentis dan GCS : E4 M6 V5 = 15

Kualitatif : Tingkah laku baik.

Orientasi : Tempat, orang, waktu, (baik)

Daya ingat : baru dan lama (baik)

Syaraf-Syaraf Otak

N I (Olfaktorius) Kanan Kiri

Daya Penghidu + +

N II (Optikus)

Daya penglihatan + +

Pengenalan warna + +

Medan penglihatan + +

N III (Okulomotorius)

Ptosis - -

Gerakan bola mata ke

Superior + +

Inferior + +

Medial + +

Ukuran pupil 3 mm 3 mm

Bentuk pupil bulat bulat

Reflek cahaya langsung + +

N IV (Troklealis)

Gerak bola mata kelateral bwh + +

Diplopia - -

N V (Trigeminus)

Menggigit + +

Membuka mulut + +

N VI (Abdusens)

Gerakan mata ke lateral + +

N VII (Facialis)

Kerutan kulit dahi + -

Kedipan mata + -

Lipatan nasolabial + -

Sudut mulut + -

Mengerutkan dahi + -

Mengerutkan alis + -

Menutup mata + -

Meringis + -

Menggembungkan pipi + -

N VIII (Akustikus)

Mendengar suara + +

N IX (Glosofaringeus)

Sengau - -

Tersedak - -

N X (Vagus)

Denyut nadi 72x/menit 72x/menit

Bersuara + +

Menelan + +

N XI (Assesorius)

Memalingkan kepala + +

Sikap bahu N N

Mengangkat bahu N N

Trofi otot bahu eutrofi eutrofi

N XII (Hipoglosus)

Sikap lidah N N

Tremor lidah - -

Menjulurkan lidah ++ -

Trofi otot lidah eutrofi eutrofi

BADAN

Trofi otot punggung : eutrofi

Nyeri membungkukkan badan : -

KOLUMNA VERTEBRALIS

Bentuk : Normal

Nyeri tekan : -

ANGGOTA GERAK ATAS

Inspeksi: Drop hand : -/-

Pitcher hand : -/-

Claw hand : -/-

Ekstremitas superior Ekstremitas inferior

Gerakan +/+ +/+

Sensibilitas +/+ +/+

Kekuatan 5/5 5/5

Biseps Triseps Radius Ulna Patella

Achilles

Reflek Fisiologi +/+ +/+ +/+ +/+

+/+ +/+

Reflek Patologis Kanan Kiri

Babinski - -

Chaddock - -

Oppenheim - -

Gordon - -

Schaefer - -

Gonda - -

Hoffman-Tromner - -

Bing - -

Rosolimo TDL TDL

MendelBedrew TDL TDL

Tes Petrick TDL TDL

Tes Kontra Petrick TDL TDL

Kernig TDL TDL

IV. RESUME

Anamnesis (subyektif)

Pasien adalah seorang laki-laki, usia 43 tahun, datang ke Poliklinik

Rehabilitasi Medik RSUD Wirosaban rujukan dari poliklinik Saraf dengan riwayat

mulut perot kesebelah kanan dan muka sebelah kiri terasa tebal, bicara cedal-cedal,

riwayat hipertensi (+), hiperkholesterolemia (+), riwayat jantung (-), trauma (-).

Pemeriksaan Fisik (Obyektif)

KU : Baik

Kesadaran : Compos Mentis GCS: 15

Vital sign : Tekanan darah : 120/80 mmHg

Denyut nadi : 72 x/menit

Pernafasan : 20 x/menit

Suhu : 36,40C

Status Internus : dalam batas normal

Status Psikis : dalam batas normal

Status Neurologik : Kesadaran : Compos Mentis, GCS : E4 M6 V5 = 15

Nervus Cranialis I-XII : dbn kecuali N. VII: Paresis N.VII kiri tipe perifer.

Motorik ekstremitas atas dan bawah : dbn

Ekstremitas Superior Ekstremitas Inferior

Gerakan +/+ + /+

Kekuatan 5/5 5/5

Tonus N N

Sensibilitas + +

Reflek fisiologis +/+ +/+

Reflek patologis -/- -/-

KESIMPULAN (Assesment)

Diagnosis klinis : Paresis N.VII kiri tipe Perifer

Diagnosis topik : Setinggi foramen stilomastoideus dekstra.

Diagnosis etiologi : Idiopatik

PLANNING

Terapi Medikamentosa:

1. Prednison selama 5 hari

2. Neurotropik 3 x 1 tab

Terapi Rehabilitasi Medik

• Fisioterapi :

- Program :

1. Infra Red 15 menit wajah kiri.

2. Elektrikal Stimulasi intensitas 1 MA

3. Latihan gerak volunteer otot wajah kiri dengan menggunakan cermin dengan

gerakan : mengerutkan dahi, menutup mata, tersenyum, bersiul/meniup,

mengangkat sudut mulut.

4. Home training 2x/hari : kompres hangat dengan handuk dan massage.

2. Ocupational Terapy

-. Program :

1. Suportif OT

2. Latihan penguatan otot pipi dan wajah kiri dengan kerut dahi, tutup mata,

tersenyum, meringis, meniup bola pingpong,/lilin, berkumur.

3. Latihan makan dengan mengunyah disisi yang lemah.

3. Psikologi

Program : Memberikan penjelasan kepada pasien bahwa kelumpuhan wajah sisi

kirinya tidak berbahaya dan pada umumnya dapat sembuh kembali.

3. Sosial Worker

Program memberikan penjelasan bahwa penyakitnya dapat disembuhkan dan

memotivasi pasien tentang perlunya latihan teratur di Unit Rehabilitasi Medis dan

dirumah.

4. Orthotic Prosthetic

Program : Dapat dipasang Y plester yang diganti tiap 8 jam.

5. Speech Terapy

Program :

1. Peningkatan gerak organ artikulasi bicara untuk ketepan dan kekuatan,

kecepatan dengan buka dan tutup mulu, meringis, diberi tahanan pada daerah yang

lemah sampai simetri, menghisap.

2. Ltihan menggembungkan pipi.

3. Meniup, mengunyah dengan mulut tertutup.

4. latiahn pengucapan yang tepat.

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 nerve’s 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.

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.)

• References

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 facial 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.

3. References

Bell Palsy Slideshow

Click the image below to see a slideshow of images for Bell Palsy.

View Ima

ge

The facial

nerve.

4. References

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 nerve’s 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.

5. References

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]

6. References

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-Barré 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]

• References

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 patient’s 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 eMedicine’s Brain

and Nervous System Center. Also, see eMedicine’s patient

education article Bell Palsy.

• References

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).

View Ima

ge

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-Barré 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

• References

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 patient’s skin for signs of

squamous cell carcinoma, which can invade the facial nerve, and

parotid gland disease.

• References

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.

• References

• 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

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 A1c 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.

• References

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]

• References

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.

• References

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.

• References

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.

• References

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.

• References

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.

• References

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.

• References

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.

• References

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).

• References

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.

• References

Histologic Findings

A review of 12 autopsy cases of patients with Bell palsy was

summarized in Peter Dyck’s 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.

• References

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.

• References

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.

• References

Local Treatment

It is universally accepted that eye care is imperative in Bell palsy.

The patient’s 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.

• References

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 author’s 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.

• References

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.

• References

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.

• References

• Medication

• Medication Summary

• Corticosteroids

• Antiviral Agents

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent

complications. Agents used in cases of Bell palsy include

corticosteroids and antivirals.

• References

• Corticosteroids

• Class Summary

• Prednisone (Deltasone, Orasone, Sterapred)

Prednisone (Deltasone, Orasone,

Sterapred)

• Dosing, Interactions, etc.

Clinical Context: 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.

• References

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.

• References

• Antiviral Agents

• Class Summary

• Acyclovir (Zovirax)

• Valacyclovir (Valtrex)

Acyclovir (Zovirax)

• Dosing, Interactions, etc.

Clinical Context: 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.

The exact cause of Bell’s palsy is still not known. Infections, immunologic and genetic factors have been suggested to play roles in the pathogenesis of the disease. The hypothesis that hypoxia and compression of the facial nerve induced by oedema in the facial canal is widely accepted7. Changes are brought about by the Herpex Simplex virus (HSV) infection8 In the contemporary times, HSV has been demonstrated in the geniculate ganglion by using molecular techniques9. This hypothesis looks more tangible when HSV antibody titres were found to be increased in sufferers of Bell’s palsy, when 2-20% of the patients has demonstrated sudden changes in the antibody titres to Herpes group of viruses (Herpez Zoster, Rubella, Cytomegalo, Adeno, Rhino, Mumps and Ebstien Barr). As the patient recovers from a primary HSV infeciton, the virus subsides in a latency phase in the various cranial and spinal nerve ganglia10 Through some poorly understood mechanism, the virus is reactivated within the ganglion cells. Circulating antibodies guard against the dissemination of the virus. This promotes local ganglionitis which may manifest clinically as hypofunction. The virus may travel up or down the axon to induce a radiculitis of a nerve plexus. It may reach brain stem to excite a local inflammatory response in terms of meningoencephalitis, which may reflect as an increased protein content in the cerebrospinal fluid3. The virus may infect the Schwaan’s cell in the nerve. It acquires a protein coat from the nerve cell as it escapes through the membrane. This operation excites an autoimmune response to the nerve-cell membrane. To

follow this phenomenon is the lymphocytic infiltration in the affected nerve fiber, leading to fragmentation of myelin, demyelination and chromatolysis of the facial nucleus3 The cell function is impaired till such time that the distal disease process resolves. Functional muscle reinnervation revive as remyelination starts. Until recently there was no agreement on the probable location of the facial nerve segment implicated in the Bell’s palsy. Magnetic resonance imaging studies procured during the course of Bell’s palsy have exhibited enhance in the labyrinthine, geniculate and the proximal tympanic segments of the facial nerve11. Entrapment at the site of meatal foramen as the principle factor has been the subject of debate since long. This happens to be the narrowest point in the fallopian canal. Vulnerable vascular channels, conduction blocakde at this point due to neuropraxic effect, MM enhancement of the segment and above all intra-operative observations favour this hypothesis12. There are counter evidences to suggest that facial nerve is not tightly contained at the meatal foramen as studied in children. This provides a possible explanation for the relative infrequency of Bell’s palsy in the young age13. Data accumulated from the cadaver and animal studies points to the fact that labyrinthine segment of the facial nerve contain fewer and smaller intrinsic blood vessels compared to the mastoid and the tympanic segments. This substantiates the contention that labyrinthine segment is the most likely site of lesion in Bell’s palsy14. Autopsy studies in the temporal bone have shown congestion and infiltration of the nerve in the internal auditory meatus. There was compression of the nerve in the proximal portion while demyelination was observed in the tympanic segment13. Interestingly histopathological analysis showed a sharp line of demarcation between sclerotic nerve proximal to and necrotic nerve distal to the meatal foramen, favouring this to be the ideal location of the lesion15.

Pregnancy

During human pregnancy, increased fetal production of cortisol between weeks 30 and 32 initiates production of fetal lung surfactant to promote maturation of the lungs. In fetal lambs, glucocorticoids (principally cortisol) increase after about day 130, with lung surfactant increasing greatly, in response, by about day 135,[7] and although lamb fetal cortisol is mostly of maternal origin during the first 122 days, 88 percent or more is of fetal origin by day 136 of gestation.[8] Although the timing of fetal cortisol concentration elevation in sheep may vary somewhat, it averages about 11.8 days before the onset of labor.[9] In several livestock species (e.g. the cow, sheep, goat and pig), the surge of fetal cortisol late in gestation triggers the onset of parturition by removing the progesterone block of cervical dilation and myometrial contraction. The mechanisms yielding this effect on progesterone differ among species. In the sheep, where progesterone sufficient for maintaining pregnancy is produced by the placenta after about day 70 of gestation,[10][11] the pre-partum fetal cortisol surge induces placental enzymatic conversion of progesterone to estrogen. (The elevated level of estrogen stimulates prostaglandin

secretion and oxytocin receptor development.) In the pregnant cow, where progesterone maintaining pregnancy is provided by the corpus luteum, luteolysis is induced by endometrial release of prostaglandin F2alpha, in response to fetal cortisol (and estrogen).[12]

[edit] Cortisol is released in response to stress, sparing available glucose for the brain, generating new energy from stored reserves, and diverting energy away from low-priority activities (such as the immune system) in order to survive immediate threats or prepare for the exertion of rising to a new day. However, prolonged cortisol secretion (which may be due to chronic stress or the excessive secretion seen in Cushing's syndrome) results in significant physiological changes.[1] Cortisol can weaken the activity of the immune system. Cortisol prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 (IL-1), and unable to produce the T-cell growth factor.[47] Cortisol also has a negative-feedback effect on interleukin-1.[48] IL-1 must be especially useful in combating some diseases; however, endotoxic bacteria have gained an advantage by forcing the hypothalamus to increase cortisol levels (forcing the secretion of CRH hormone, thus antagonizing IL-1). The suppressor cells are not affected by glucosteroid response-modifying factor (GRMF),[49] so the effective setpoint for the immune cells may be even higher than the setpoint for physiological processes (reflecting leukocyte redistribution to lymph nodes, bone marrow, and skin). Rapid administration of corticosterone (the endogenous Type I and Type II receptor agonist) or RU28362 (a specific Type II receptor agonist) to adrenalectomized animals induced changes in leukocyte distribution. Natural killer cells are not affected by cortisol.[50]

Eighty-four patients were examined for blood coagulability during the acute phase of Bell's palsy. Abnormally high levels of

thrombin-antithrombin III complex (TAT) and alpha-2 plasmin

inhibitor-plasmin complex (PIC) were found, with these increases statistically significant. Values tended to be higher in patients

within 3 days after occurrence of the palsy when compared to

values in patients 4 days or more later. Abnormal TAT and PIC levels in the acute phase then tended to become normalized

during the convalescent phase of the disease. These findings

indicated that activation of intravascular coagulability had occurred, with patients entering a temporary clot-forming state.

Among the several hypotheses for the etiology of Bell's palsy, our

findings support a circulation disorder as an influential factor. Pre-eclampsia is a potentially lethal complication of pregnancy. Sometimes

called, "Toxemia of Pregnancy," pre-eclampsia is characterized by high blood

pressure and protein in the urine after the 20th week of pregnancy. Other symptoms include swelling (edema) and weight gain.

As the disease progresses, it is usually accompanied by some or all of the following: headache, visual disturbances, abdominal pain, decreased urine

output and nausea/vomiting. If untreated, it can progress to eclampsia, a very serious disease that causes seizures, brain herniation and liver rupture.