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Bells Palsy: To Treat or Not to Treat

K. Kevin Ho, M.D. Shawn D. Newlands, M.D., Ph.D., M.B.A. University of Texas Medical Branch at Galveston Grand Rounds Presentation February 14, 2007

Historical Perspectives
Sir Charles Bell (1774-1842)
Studied facial anatomy extensively during Battle of Waterloo Concluded that facial nerve controlled facial expression Respiratory nerve of the Face

Anatomy

Bells Palsy
Idiopathic facial paralysis Diagnosis of Exclusion Most common diagnosis (> 60%) for acute facial palsy 30 per 100,000 Peripheral neuropathy Generally unilateral Rapid onset < 48 hours

Age Distribution
2002

Peitersen E. Acta Otolaryngol 2002;549:430. Peitersen E. Am. J. Otology. 1982

Complete Remission & Age


90 84 75

64

36

0-14

15-29

30-44 Age 45-59

> 60

Peitersen E. Acta Otolaryngol 2002;549:430.

Return of Muscular function


85 %

Months
Peitersen E. Acta Otolaryngol 2002;549:430.

Time of beginning remission & Sequelae

Peitersen E. Am. J. Otology. 1982

Complete Recovery
71

Peitersen E. Acta Otolaryngol 2002;549:430.

Incomplete vs. Complete

Peitersen E. Acta Otolaryngol 2002;549:430.

Symptomatology
Reduced Stapedial reflex Complete palsy @ presentation Tear flow Post-auricular pain Dysgeusia Hyperacusis
Peitersen E. Acta Otolaryngol 2002;549:430.

71% 69% 67% 52% 34% 14%

Predicting Muscular Sequelae


91 83 % Muscular Sequelae 63 91 Abnormal

Normal

27

5 Taste Stapedial Lacrimation

Peitersen E. Acta Otolaryngol 2002;549:430.

Favorable prognosis for full recovery


Incomplete palsy Early recovery Young patients Normal taste, stapedial reflex, lacrimation Lack of post-auricular pain
Peitersen E. Acta Otolaryngol 2002;549:430.

Pathophysiology
Exact etiology unknown Viral infection
Herpes Simplex

Vascular ischemia Autoimmune disorder Hereditary

Role of HSV-1

Murakami: Ann Intern Med, Volume 124(1).January 1, 1996.27-30

Diabetes Mellitus
Bells patients with DM
14 % (Korczyn AD 71) 21 % (Alford BR 71) 38 % (Yasuda K 75)

66% demonstrate glucose intolerance Functional recovery poorer in diabetics

Pregnancy
Incidence of Bells palsy 3-4 x higher
(Hilsinger, Cohen et al.)

Third trimester with highest risk Higher risk of complete palsy Lower chance of complete recovery
(Gillman et al.)

Preeclampsia 6 x prevalence in pregnant women with facial palsy

Differential Diagnosis Acute facial palsy


Infection Herpes Zoster Oticus (Ramsey Hunt Syndrome) Lyme disease Acute Otitis media +/- mastoiditis Congenital Treacher Collins syndrome Mobius syndrome Trauma Temporal Bone fracture Barotrauma Metabolic Diabetes Hypothyroidism Vascular Benign intracranial hypertension Neoplasm Facial neuroma Acoustic neuroma Toxic Thalidoide Iatrogenic

Early Grading System

Peitersen E. Am. J. Otology. 1982

House-Brackman Grading System

MRI

Post-GAD Pre-GAD
Kinoshita T et al. Clin. Radiology 2001; 56: 926-32

Contrast Enhancement: Bells Palsy vs. Control


Bells Palsy

Control

Kinoshita T et al. Clin. Radiology 2001; 56: 926-32

Topognostic Test
Lacrimal
Schirmers Test

Stapedial reflex Taste Salivary flow

Electrical Test
Nerve Excitation test Maximal Stimulation test Electroneurography Electromyography (NET) (MST) (ENoG) (EMG)

Sunderland classification of peripheral nerve injury


Neurapraxia

Axonotmesis

Neurotmesis

Electroneurography (ENoG)
Transcutaneous stimulation (Evoked EMG) Compound muscle action potential (CMAP) Most useful in acute phase within 3 days 3 weeks of palsy But no info on class of injury (axonotmesis vs. neurotmesis)

Time course of Degeneration

Gantz: Laryngoscope, Fisch U. Am Volume J. Otology. 109(8).August 1984 1999.1177-1188

Fisch 1984

Fisch U. Am J. Otology. 1984

Electromyography (EMG)
Recording of voluntary muscle action potentials by needles electrodes Does not differentiate axonotmesis & neurotmesis More useful 2-3 weeks after onset of complete paralysis Perform EMG if ENoG > 95% degeneration

EMG Interpretation
Active voluntary motor units (MU)
Intact motor axon

Myogenic fibrillation potention & Absent voluntary MU


Complete nerve degeneration Partial degeneration Regenerating nerve

Fibrillation + MU

Polyphasic MU

Management of Bells Palsy


Observation Medical Treatment
Steroid Anti-viral agents Decompression Dynamic vs. static reanimation

Surgery

Facial Rehabilitation

Cochrane review on Efficacy of steroids


4 trials of 179 patients Trial 1: Cortisone vs. placebo Trial 2: Prednisone + vitamins vs. vitamins Trial 3: High dose prednisone vs. saline Trial 4: Methylprednisolone Primary endpoint: VII recovery @ 6 mos Conclusions: NO significant benefit for giving steroids to Bells palsy patients Drawbacks: Individual studies underpowered. Steroid regimens differ.

Efficacy of Steroid treatment


Prospective RCT 56 patients Arm I: Steroids Arm II: Placebo Success = HB I or II F/u @ 3 and 6 weeks No significant difference in response in the 2 groups
Turk-Boru U et al. Kulak Burun Bogaz Ihtis Derg. 2005;14(3-4):62-6.

Steroids in Complete paralysis Meta-analysis of 3 prospective trials


230 patients with HB VI

Treatment within 7 days of onset Total prednisone dose > 400 mg (405-425 mg) Complete Recovery: HB VI I
Steroid group has 17% higher rate of CR than control (placebo/ no treatment)
Ramsey MJ et al. Laryngoscope 2000; 110: 335-341

Steroid vs. Steroid + Acyclovir


Double-blind RCT 99 Bells palsy patients 53 treated with acyclovir- prednisone 46 with placebo prednisone Prednisone dose 400 mg five times daily x 10 days Combined therapy is better in terms of: Return of muscle motion Prevention of partial nerve degeneration
Adour KK 1996 Ann Otol Rhinol Laryngol. 1996 May;105(5):371-8

Steroid vs. Steroid + Acyclovir

Prednisolone Prednisolone + Valacyclovir

Prospective RCT of 150 patients Prednisolone (20 tid x 5d, 10 tid x 3 d, 10 qD x 2 d) Predisolone + Valacyclovir (500 bid x 5 d) No significant difference in recovery

Kawaguchi: Laryngoscope, Volume 117(1).January 2007.147-156

Timing of Medical Treatment

Hato N. Otol & Neurotol: 24(6) 2003

Sample Treatment
Corticosteroids
Prednisone 60 mg PO daily x 5 days, taper

Anti-viral

Valacyclovir 1000 mg PO TID


Glasses/ Sunglasses/ avoid contact lens Artificial tears, lacrilube Taping Gold weight to upper eyelid Opthalmologic consultation

Eye care

Pensak ML. Assessment and Management of the Paralyzed face. Otol. & Neurotol. Update. Nov 2006

Surgical Decompression
Middle Fossa Transmastoid Translabyrinthine Retrolabyrinthine Retrosigmoid

History of Surgical Decompression

Adour KK. 2002 Jan;259(1):40-7

Anatomy of Facial Canal

Tympanic 1.53 mm

Labyrinthine 1.02 mm 0.68 mm

Mastoid 1.48 mm

Coker NJ. Atlas of Otologic Surgery p.339

Controversy over Surgical Decompression In favor of:


Gantz BJ 99 Sillman JS 92 Huges GB 88 Goin DW 82 Fisch U 81 Brackmann DE 80 Giancarlo HR 70

Against:
Adour KK 01 Aoyagi M 88 May M 84 Gacek RR 81 McNeill R 74 Adour KK 71 Mechelse K 71

Results of Middle Fossa Approach


Grade I II III IV Iowa 3 7 1 0 Michigan 5 2 1 1 Baylor 0 6 0 0 Total 8 15 2 1

Gantz: Laryngoscope, Volume 109(8).August 1999.1177-1188

Michigan Study: MCF vs. Steroids


70 60 50 40 30 20 10 0 I II III IV

Steroids MCF

Grade
Glasscock M, Shambaugh G: Facial nerve surgery. In Surgery of the ear, 1990:434-465.

Early MCF

Gantz: Laryngoscope, Volume 109(8).August 1999.1177-1188

Timing of Decompression

Gantz: Laryngoscope, Volume 109(8).August 1999.1177-1188

Algorithm

Gantz: Laryngoscope, Volume 109(8).August 1999.1177-1188

Factors to consider for Surgical Decompression Age Comorbidities ENoG


Endpoint Progression / velocity of degeneration

Days from onset of paralysis Return of muscle function

Thank you