Bells palsy

DEFINISI Bells palsy merupakan paresis nervus fasialis perifer yang penyebabnya tidak diketahui (idiopatik) dan bersifat akut. Banyak yang mencampuradukkan antara Bells 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. Bells palsy adalah kelumpuhan fasialis perifer yang belum diketahui penyebabnya, bisa akibat proses non-supuratif, nonneoplasmatik, 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 Bells palsy secara pasti sulit ditentukan. Data yang dikumpulkan dari 4 buah Rumah sakit di Indonesia didapatkan frekuensi Bells 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 Bells palsy, tetapi ada 4 teori yang dihubungkan dengan etiologi Bells 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 Bells 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 Bells palsy terjadi akibat reaksi imunologi terhadap infeksi virus yang timbul sebelumnya atau sebelum pemberian imunisasi. D. PATOFISIOLOGI Apapun sebagai etiologi Bells palsy, proses akhir yang dianggap bertanggungjawab atas gejala klinik Bells 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. Bells 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 Bells 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 Bells 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 Istirahat 20 Mengerutkan dahi 10 Menutup mata 30 Tersenyum 30 Bersiul 10

Skor

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 : Kelain Gangguan Hiposekre an Gangguan Hiposekre Letak Lesi pengecap si motori pendengaran si saliva an lakrimalis k

Pons-meatus + akustikus + + tuli/hiperaku + internus sis Meatus akustikus + internus+ + + Hiperakusis ganglion genikulatum Ganglion + genikulatum- + + + Hiperakusis N. Stapedius N.stapediuschorda + + + + tympani Chorda + + + tympani Infra chorda tympanisekitar + foramen stilomastoideu s 5. Diagnosa etiologi : Sampai saat ini etiologi Bells 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 Bells palsy adalah untuk mengurangi/mencegah paresis menjadi bertambah dan membantu mengatasi problem sosial serta psikologinya agar penderita tetap dapat melaksanakan aktivitas kegiatan sehari-hari. Programprogram 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, Bells 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 Bells 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.

BELLS PALSY (Syaraf)

Dibuat oleh: Hariadi Supanto,Modifikasi terakhir pada Sat 29 of May, 2010 [04:52 UTC] PRESENTASI KASUS PASIEN POLIKLINIK REHABILITASI MEDIK BELLS PALSY

Anamnesis No. CM Jam Ruang

: Autoanamnesis : 110856 : 08.45 WIB : Poliklinik Rehabilitasi Medik

I.

IDENTITAS PASIEN Nama Umur : Tn. A : 43 tahun

Jenis Kelamin Alamat Pekerjaan Agama

: Laki-laki : Kauman, Mangunsari, Salatiga : PNS : Islam

II.

DATA SUBYEKTIF : Mulut perot ke kanan dan muka sebelah kiri terasa

Keluhan Utama 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 (-), Jantung (-) Riwayat Penyakit Keluarga penyakit serupa. : : : : Hipertensi (+) hiperkolestrolemia (+), DM (-) trauma : Tidak ada anggota keluarga yang menderita

Riwayat sosial ekonomi : Pasien adalah seorang Pegawai Negeri Sipil dengan gaji rata-rata Rp. 2.000.000,00/bulan III. A. DATA OBYEKTIF Status present Tekanan darah Denyut nadi Pernafasan Suhu B. Status Internus Kepala : Mesosepal, bentuk simetris. : 120/80 mmHg : 72 x/menit : 20 x/menit : 36,40C

Leher

: Pembesaran kelenjar limfe (-), kaku kuduk (-), bentuk vertebra normal, nyeri tekan vertebra (-).

Dada Abdomen C. Status Psikis

: Jantung dan Paru dalam batas normal : Hepar dan lien dalam batas normal.

Dalam batas normal D. Status Neurologis : Compos Mentis dan GCS : E4 M6 V5 = 15 : Tingkah laku baik. : Tempat, orang, waktu, (baik)

Kesadaran Kualitatif Orientasi

Daya ingat : baru dan lama (baik)

Syaraf-Syaraf Otak N I (Olfaktorius) Daya Penghidu Kanan + + Kiri

N II (Optikus) Daya penglihatan Pengenalan warna Medan penglihatan N III (Okulomotorius) Ptosis Gerakan bola mata ke Superior Inferior Medial Ukuran pupil Bentuk pupil Reflek cahaya langsung + + + 3 mm bulat + + + + 3 mm bulat + + + + + + +

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 Bersuara Menelan N XI (Assesorius) 72x/menit + + 72x/menit + + + +

Memalingkan kepala Sikap bahu Mengangkat bahu Trofi otot bahu N XII (Hipoglosus) Sikap lidah Tremor lidah Menjulurkan lidah Trofi otot lidah

+ N N eutrofi

+ N N eutrofi

N ++ eutrofi

N eutrofi

BADAN Trofi otot punggung Nyeri membungkukkan badan KOLUMNA VERTEBRALIS Bentuk Nyeri tekan :: Normal : eutrofi :-

ANGGOTA GERAK ATAS Inspeksi: Drop hand Pitcher hand Claw hand : -/: -/: -/-

Ekstremitas superior Gerakan Sensibilitas Kekuatan +/+ +/+ 5/5

Ekstremitas inferior +/+ +/+ 5/5

Biseps Achilles +/+ Reflek Fisiologi +/+ +/+

Triseps +/+

Radius +/+

Ulna +/+

Patella

Reflek Patologis Babinski Chaddock Oppenheim Gordon Schaefer Gonda Hoffman-Tromner Bing Rosolimo MendelBedrew Tes Petrick Tes Kontra Petrick Kernig

Kanan TDL TDL TDL TDL TDL

Kiri TDL TDL TDL 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 Kesadaran Vital sign : Baik : Compos Mentis GCS: 15

: Tekanan darah Denyut nadi Pernafasan Suhu

: 120/80 mmHg : 72 x/menit : 20 x/menit : 36,40C : dalam batas normal

Status Internus 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 Gerakan Kekuatan Tonus Sensibilitas Reflek fisiologis Reflek patologis +/+ 5/5 N + +/+ -/-

Ekstremitas Inferior + /+ 5/5 N + +/+ -/-

KESIMPULAN (Assesment) Diagnosis klinis Diagnosis topik Diagnosis etiologi : Paresis N.VII kiri tipe Perifer : Setinggi foramen stilomastoideus dekstra. : Idiopatik

PLANNING Terapi Medikamentosa: 1. 2. Prednison selama 5 hari Neurotropik 3 x 1 tab

Terapi Rehabilitasi Medik Fisioterapi : Program : 1. 2. Infra Red 15 menit wajah kiri. 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. 3. Latihan makan dengan mengunyah disisi yang lemah. 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. 3. 4. Ltihan menggembungkan pipi. Meniup, mengunyah dengan mulut tertutup. 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 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.

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-motorneuron 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. The facial View Ima nerve. ge 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 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. 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, EpsteinBarr 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-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 1530 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 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. 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). Left-sided Bell View Ima palsy. ge 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 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 patients 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 810 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 motionanalysis 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 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. 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 19662008 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 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. 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 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. 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 Bells 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 Bells 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 Schwaans 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 Bells palsy. Magnetic resonance imaging studies procured during the course of Bells palsy have exhibited enhance in the labyrinthine, geniculate and the proximal tympanic segments of the facial nerve 11. 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 intraoperative 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 Bells 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 Bells 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 negativefeedback 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.