bell's palsy - utmb health

Viet Pham, MD

Dayton Young, MD

Tomoko Makishima, MD, PhD

The University of Texas Medical Branch (UTMB Health)

Department of Otolaryngology

Grand Rounds Presentation

October 29, 2012

Bell’s Palsy

All images obtained via Google

search unless otherwise specified.

All images used without

permission.

Diagnostic and Treatment Considerations

(ww

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.net)

Anatomy

Pathophysiology

Diagnostics

Treatment

Conclusions

Outline

Before Bell’s Palsy After Bell’s Palsy

Contains 7,000-10,000 fibers

Nuclei

Somatic – Motor

Taste – Tractus solitarius

Secretomotor – Superior salivatory

Segments

Intracranial (cisternal)

Meatal

Labyrinthine

Tympanic

Mastoid

Extratemporal

Facial Nerve Anatomy

(J Neurol Neurosurg Psychiatry 2001;71:149-154)

Facial Nerve Segments

(www.entusa.com)

Intracranial

Meatal

Labyrinthine

Tympanic

Mastoid

Extratemporal

Intracranial

Meatal

Labyrinthine

Tympanic

Mastoid

Extratemporal


(radiopaedia.org) (info.med.yale.edu)

Intracranial

Meatal

Labyrinthine

Tympanic

Mastoid

Extratemporal


Internal auditory canal (IAC)

8mm

Zero branches

(Lalw

ani A

K,

ed. C

urr

ent D

iagnosis

and T

reatm

ent:

Oto

lary

ngolo

gy H

ead a

nd N

eck S

urg

ery

, 2nd E

d.)

Intracranial

Meatal

Labyrinthine

Tympanic

Mastoid

Extratemporal


IAC to geniculate ganglion

3-4mm

Three branches from geniculate ganglion

(Lalw

ani A

K,

ed. C

urr

ent D

iagnosis

and T

reatm

ent:

Oto

lary

ngolo

gy H

ead a

nd N

eck S

urg

ery

, 2nd E

d.)

Intracranial

Meatal

Labyrinthine

Tympanic

Mastoid

Extratemporal


Geniculate ganglion to pyramidal eminence

8-11mm

Zero branches

(Lalw

ani A

K,

ed. C

urr

ent D

iagnosis

and T

reatm

ent:

Oto

lary

ngolo

gy H

ead a

nd N

eck S

urg

ery

, 2nd E

d.)

Intracranial

Meatal

Labyrinthine

Tympanic

Mastoid

Extratemporal


Pyramidal eminence to stylomastoid foramen

8-14mm

Three branches

Intracranial

Meatal

Labyrinthine

Tympanic

Mastoid

Extratemporal


Stylomastoid foramen to major branches

15-20mm

(www.facialparalysisinstitute.com)

House-Brackmann Scale

Grade Appearance Forehead Eye Mouth

I normal normal normal normal

II slight weakness

normal resting tone

moderate to good

movement

complete closure

minimal effort slight asymmetry

III non-disfiguring weakness

normal resting tone

slight to moderate

movement

complete closure

maximal effort

slight weakness

maximal effort

IV disfiguring weakness

normal resting tone none incomplete closure

asymmetric with

maximal effort

V minimal movement

asymmetric resting tone none incomplete closure slight movement

VI asymmetric none none none

(House 1985)

Grade Appearance Synkinesis

I normal normal

II slight weakness

normal resting tone

synkinesis barely noticeable

contracture or spasm absent


normal resting tone

obvious but not disfiguring synkinesis

mass movement or spasm present


normal resting tone severe synkinesis, mass movement, or spasm

V minimal movement

asymmetric resting tone synkinesis, contracture, and spasm usually absent

VI asymmetric no synkinesis, contracture, or spasm

Grade Appearance Forehead Eye Mouth

I normal normal normal normal

II slight weakness

normal resting tone

moderate to good

movement

complete closure

minimal effort slight asymmetry


normal resting tone

slight to moderate

movement

complete closure

maximal effort

slight weakness

maximal effort


normal resting tone none incomplete closure

asymmetric with

maximal effort

V minimal movement

asymmetric resting tone none incomplete closure slight movement

VI asymmetric none none none

House-Brackmann Scale (House 1985)

Grade Appearance Synkinesis

I normal normal

II slight weakness

normal resting tone

synkinesis barely noticeable

contracture or spasm absent


normal resting tone

obvious but not disfiguring synkinesis

mass movement or spasm present


normal resting tone severe synkinesis, mass movement, or spasm

V minimal movement

asymmetric resting tone synkinesis, contracture, and spasm usually absent

VI asymmetric no synkinesis, contracture, or spasm

House-Brackmann Scale (House 1985)

Sir Charles Bell first described facial paralysis in 1818

Acute but limited facial paralysis

Rapid onset

Few associated symptoms

Spontaneous recovery

Most common diagnosis for facial

nerve palsy

Diagnosis of exclusion

Historically thought to be idiopathic

Herpes simplex virus (HSV) reactivation

Bell’s Palsy

(BMJ 2004; 329(7465):553–557.)

Incidence of 30 per 100,000

Pregnant females (3.3 times greater)

Diabetics (4-5 times greater)

Equal gender distribution in middle age

Females, 10-19 years (twice as common)

Males, > 40 years (1.5 times greater)

Equal unilaterality

Bilateral involvement in less than 1%

Recurrence rate of 10%

Positive family history in 10%

Bell’s Palsy Demographics

Outcomes of 1011 untreated patients (Peiterson 1982)

Mean age between 40-44 years

Less common before 15 years and

after 60 years

No gender predilection

Recurrence in 6-9%

Bell’s Palsy Natural History


Paresis alone

Occured in 31%

Complete recovery in 95%

Complete unilateral paralysis in 69%

Some recovery by 3 weeks (85%)

House-Brackmann 1 in 71%

House-Brackmann 2 in 13%

House-Brackmann 3-5 in 16%


George Clooney, circa middle school


Complete recovery by one month in 85%

Progression to complete degeneration in 15%

Signs of recovery after 3-6 months

Sequelae associated with longer recovery

Diminished function

Contracture with movement

Tearing



Reduced stapedial reflex

Postauricular pain

Dysgeusia

Decreased lacrimation

Phonophobia

Bell’s Palsy Associated Symptomatology

Historically thought to be idiopathic

Two theories

Vascular congestion

Viral polycranioneuropathy

Bell’s Palsy Pathophysiology

Autonomic vascular instability (Mcgovern 1955)

Spasm of nutrient arterioles

Secondary ischemia

Nerve edema

Compression within

fallopian canal

Possible triggers

Cold temperature

Psychosomatic

Pathophysiology Vascular Congestion

Acute infectious polyneuritis cerebralis

acusticofacialis by Antoni in 1919 (Freidman 2000)

Facial nerve edema from viral

inflammatory response

HSV proposed etiology in 1972 (McCormick)

Pathophysiology Infectious

(www.facialnervecenter.org)

Burgess (1994)

Surgita (1995)

Murakami (1996)

Furuta (1998)


Burgess (1994)

Surgita (1995)

Murakami (1996)

Furuta (1998)


Patient who died six days after

developing Bell’s palsy

HSV type 1 (HSV-1) DNA in temporal

bone section

Burgess (1994)

Surgita (1995)

Murakami (1996)

Furuta (1998)


Inoculation of mice with HSV-1 DNA

Auricle in 104

Tongue in 30

Transient facial paresis

Began 6-9 days after inoculation

Spontaneous recovery after 3-7 days

Histopathology

Neural edema

Inflammatory cell infiltration

Vacuolar degeneration

HSV antigens

Beginning 6-20 days after inoculation

Facial nerve, geniculate ganglion, and

facial nerve nucleus

Burgess (1994)

Surgita (1995)

Murakami (1996)

Furuta (1998)


Transmastoid decompression during

active phase of disease

HSV-1 in endoneural fluid of 11 out of 14

with Bell’s palsy

No varicella-zoster virus (VZV)

No Epstein Barr

Ramsay Hunt

VZV present

No HSV-1

Trauma or neoplasm

No HSV-1

No VZV

Burgess (1994)

Surgita (1995)

Murakami (1996)

Furuta (1998)


Polymerase chain reaction of saliva

Bell’s palsy in 47

Ramsay Hunt in 24

Healthy, HSV-positive in 16 (control)

HSV-1

In 50% with Bell’s palsy

In 19% of controls

Testing within 7 days

HSV-1 in 40% of Bell’s palsy

HSV-1 in 7% of Ramsay Hunt

HSV-1 usually undetectable by second

week

McKeever (1987)

Lymphocytic infiltrate

Myelin degeneration

Most pronounced at labyrinthine segment

And perineural edema (Donoghue 1983; Podvinec 1984)

Facial nerve entrapped at meatal foramen (Fisch 1983)

Conductive block at this site (Gantz 1982)

Ischemia with increased or prolonged constriction

Wallerian degeneration results

Axonotmesis

Neurotmesis

Pathophysiology Histolopathology

(Lalwani AK, ed. Current Diagnosis and Treatment:

Otolaryngology Head and Neck Surgery, 2nd Ed.)

History

Physical examination

Radiology

Topography

Audiology

Electrophysiology

Bell’s Palsy Diagnostics

Hearing loss or vertigo

Timing

Sudden onset

Evolution over 2-3 weeks

Presence of ear disease

Vesicular eruption

Bilateral

Recurrence

Diagnostics History and Physical Examination

Symmetric audiological function

Absent ipsilateral acoustic reflex

Bell’s palsy questioned if vertiginous

Clinical threshold for cerebrovascular accident


Timing

Sudden onset



Vesicular eruption

Bilateral

Recurrence



Timing

Sudden onset



Vesicular eruption

Bilateral

Recurrence


Occurs over 24-48 hours

Can progress to complete paralysis over 1-7 days

Rule out neoplasm if evolution past 3 weeks


Timing

Sudden onset



Vesicular eruption

Bilateral

Recurrence


Chronic otitis media

Cholesteatoma


Timing

Sudden onset



Vesicular eruption

Bilateral

Recurrence


Ramsay-Hunt syndrome


Timing

Sudden onset



Vesicular eruption

Bilateral

Recurrence


Guillain-Barre syndrome

Lyme disease

Intracranial neoplasm

(ent.uci.edu)


Timing

Sudden onset



Vesicular eruption

Bilateral

Recurrence


Usually excludes Bell’s palsy

Melkersson-Rosenthal syndrome

(Rev B

ras O

torr

inola

ringol 2002; 68(5

):755

-760)

Localize lesion

Computed tomography

Trauma

Mastoiditis

Cholesteatoma

Magnetic resonance imaging (MRI)

Nerve enhancement

No correlation with site or degree of enhancement

Exclude neoplasm

Diagnostics Radiology

Schirmer test → greater superficial petrosal

Stapedial reflex → stapedial branch

Electrogustometry → chorda tympani

Salivary flow → chorda tympani

Unable to predict location or outcome

Diagnostics Topography

Evaluate for pathology of eighth cranial nerve

Bell’s palsy

Symmetric audiological function

Absent ipsilateral acoustic reflex

Retrocochlear pathology

Asymmetrical thresholds

Acoustic reflex decay

Diagnostics Audiology

Diagnostics Electrophysiology

Provides prognostic information

Not used for paresis only

Initiated 3 days after progression to complete paralysis

Tests

Nerve excitability test (NET)

Maximum stimulation test (MST)

Electroneuronography (ENoG)

Electromyography (EMG)

Nerve injury

Neuropraxia: conduction block but with axonal continuity

Axonotmesis: axoplasmic disruption but endoneural sheath

preservation

Neurotmesis: disruption of axonal and supportive cells

Test results

Neuropraxia

Axonotmesis

Neurotmesis


Nerve injury



preservation


Test results

Neuropraxia

Axonotmesis

Neurotmesis


NET, MST, and ENoG normal

No voluntary motor action potentials on EMG

Nerve injury



preservation


Test results

Neuropraxia

Axonotmesis

Neurotmesis


NET, MST, and ENoG with rapid and complete degeneration

EMG

No voluntary motor action potentials

Myogenic fibrillation potentials after 10-14 days

Nerve injury



preservation


Test results

Neuropraxia

Axonotmesis

Neurotmesis


Similar results as axonotmesis

Less predictable outcome

Cannot differentiate between the two

Described by Hilger in 1964

Compare thresholds for minimal muscle contraction

Normal side

Paralyzed side

Difference of 3.5mA

Severe degeneration

Higher likelihood of poorer outcome

Inaccurate within first 3 days of Bell’s palsy onset

Subjective comparison

Electrophysiology Nerve Excitability Test

Compare facial movement with maximum stimulation

Greater degree of weakness with worsening degeneration

Inaccurate within first 3 days of Bell’s palsy onset

Subjective comparison

Electrophysiology Maximum Stimulation Test

Compares compound action potential of both sides

Stimulate nerve at stylomatoid foramen

Measure muscular response near nasolabial groove

Less intact motor axons with

Wallerian degeneration

Worse prognosis with rapid

degeneration

Inaccurate within first 3 days of

Bell’s palsy onset

Quantitative analysis,

observer independent

Electrophysiology Electroneuronography

(Am J Otol 1992; 13:127–133.)

Esslen (1977)

Full recovery in 88% if < 90% degeneration

Full recovery in 30% if 90-95% degeneration

No full recovery if 100% degeneration

Fisch (1981)

Satisfactory spontaneous recovery if < 90% degeneration within 3

weeks of onset

High likelihood of 95% degeneration if reach 90% degeneration

Permanent unsatisfactory result in 50% with 95-100% degeneration

within 2 weeks of onset

Electrophysiology Electroneuronography

Measure action potentials with volitional movement

Silence

Resting state

Muscle atrophy or fibrosis

Early acute paralysis

Diphasic or triphasic with normal contraction

Fibrillation indicates degeneration

Polyphasic indicates reinnervation

Electrophysiology Electromyography

Quantitative analysis, observer independent

Complementary test with ENoG

Regenerating nerve fibers do not complete a summation potential on

ENoG

Degeneration if myogenic fibrillation potentials but no voluntary

motor units on EMG

Regeneration if both defibrillation potentials and motor units on EMG

No fibrillation potentials until 10-14 days after onset

Unable to distinguish between total neuropraxic injury and

regenerating nerve in acute phase

Electrophysiology Electromyography

Observation

Monitor progression

Eye care

Medical

Steroids

Antivirals

Surgical

decompression

Treatment

(www.vgcats.com)

Typically start prednisone 1mg/kg/d up to 70-80mg

Usually taper after 5-7 days

May extend therapy if no improvement

Some benefit with steroids (Adour 1972; Katusic 1986)

If combined with antivirals (de Almeida 2009)

Optimal effect with early intervention (Brown 1982; Williamson 1996)

Prednisolone within 24 hours (Shafshak 1994)

Prednisone (Austin 1993)

Randomized, double-blind, placebo-controlled

Improved recovery with prednisone

Statistically insignificant trend for denervation prevention

Treatment Steroids Beneficial

Ramsey (2000)

Meta-analysis of 27 prospective and 20 retrospective trials

Three met inclusion criteria (1975-1994)

Prospective, controlled trials

Prednisone ( >400mg) started within 7 days of onset

Steroids improved complete recovery by 17%

Generally positive benefit from excluded trials

Complete recovery 49-97% with steroids

Complete recovery 23-64% without

Cochrane Review: steroids increase frequency of complete

recovery (Salinas, 2010)

Treatment Steroids Beneficial

No evidence of benefit (May 1976; Stankiewitz 1987)

Literature review (Grogan 2001)

Nine studies compared steroids to placebo (1954-1999)

No difference in recovery or synkinesis

Most studies underpowered

Beneficial trend in some studies

Probable benefit with steroids

Treatment Steroids Not Beneficial

No benefit in children (Prescott 1987)

Pediatric literature review (Salman 2001)

Eight trials and one review (1966-1998)

Five randomized

Prednisone or corticotropin

Only one exclusively studied children

Benefit reported in four trials

No statistical sub-analysis in all trials

Heterogeneity precluded meta-analysis or recommendation

Treatment Steroids Not Beneficial

Prednisone & acyclovir (Adour 1996)

Double-blind with prednisone and acyclovir or placebo

Therapy within 3 days of onset

Prednisone & acyclovir

Less facial weakness on MST

Less unsatisfactory recovery

Prednisone alone better than acyclovir alone (De Diego 1998)

Literature review (Grogan 2001)

Three studies on antivirals (1992-1998)

Acyclovir vs prednisone; acyclovir & prednisone vs prednisone

Lack of studies to establish benefit

Possible benefit with adding acyclovir to prednisone

Treatment Antivirals

Prednisone & valacyclovir vs no treatment (Axelsson 2003)

Improved complete recovery (87.5% vs 68%)

Less House-Brackmann IV or worse (1.8% vs 18%)

Complete recovery in >60 years (100% vs 42%)

Prednisolone & valacyclovir vs placebo (Hato 2007)

Prospective, randomized placebo-controlled

Six academic tertiary care centers

222 patients

Improved recovery rate with valacyclovir (96.5% vs 89.7%)

Cochrane Review (Lockhart 2009)

Antivirals plus steroids beneficial over placebo alone

Antivirals alone not beneficial over steroids or placebo alone

Treatment Antivirals

(Bra

ckm

ann 2

010)

First described in 1932 by Balance & Duel

Stylomastoid foramen in 1930’s

Tympanic segment in 1960’s

Decompression beneficial (Giancarlo 1970)

No benefit with decompression from geniculate ganglion to

stylomastoid foramen (McNeill 1974)

Transmastoid

Decompression may be beneficial (May 1979)

From geniculate to labyrinthine segment

Meatal foramen was not decompressed

No benefit from transmastoid approach within 14 days (May 1984)

No benefit with decompressing mastoid segment alone (May 1985)

Treatment Surgical

(Bra

ckm

ann 2

010)

Fisch (1972)

Total nerve decompression via middle cranial fossa and

transmastoid approach

Conduction block proximal to geniculate ganglion

ENoG with 90% degeneration

Decompress meatal foramen within 3 weeks (Fisch 1981)

Decompression within 2 weeks (Gantz 1999)

Steroids if ENoG with <90% degeneration, no antivirals

Decompress if ENoG with >90% degeneration & no EMG activity by 2

weeks

Treatment Surgical

(Bra

ckm

ann 2

010)

Multicenter study, surgery vs steroids

Middle cranial fossa

Decompress internal auditory canal through tympanic segment

Surgical control if decompress after 2 weeks of paralysis

Improved outcomes if decompress within 2 weeks

House-Brackmann recovery I/II (91% vs 42% steroids) by 7 months

House-Brackmann recovery III/IV (9% vs 58% steroids) by 7 months

Similar results between surgical control and steroid groups

House-Brackmann recovery I/II in all with ENoG <90%

degeneration

Treatment Surgical (Gantz 1999)

Treatment Algorithm

(Brackmann 2010)

Most common diagnosis of facial paralysis

Diagnosis of exclusion

Prognostic information with electrophysiology

Medical therapy

Steroids

Antivirals

Surgical

decompression

ENoG with

>90% degeneration

No voluntary EMG activity within 14 days of paralysis

Conclusion

(www.explosm.net)

References

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prednisone alone: a double blind, randomized controlled trial. Ann Otol Rhinol Laryngol 1996; 105:371-378.

Adour KK, Wingerd J, Bell DN, et al. Prednisone treatment for idiopathic facial paralysis (Bell’s palsy). N Engl J Med 1972;

287:1268-1272.

Austin JR, Peskind SP, Austin SG, et al. Idiopathic facial nerve paralysis: a randomized double blind controlled study of

placebo versus prednisone. Laryngoscope 1993; 103:1326-1333.

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palsy. Ann Otol Rhinol Laryngol 2003; 112:197-201.

Ballance C, Duel AB. The operative treatment of facial palsy: by the introduction of nerve grafts into the fallopian canal and by

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Burgess RC, Michaels L, Bale JF. Polymerase chain reaction amplification of herpes simplex viral DNA from the geniculate

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de Almeida JR, Al Khabori M, Guyatt GH, et al. Combined corticosteroid and antiviral treatment for Bell palsy: a systematic

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de Diego J I, Prim MP, De Sarriá MJ, et al. Idiopathic facial paralysis: A randomized, prospective, and controlled study using

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References

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54:162-166.

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References

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86:1111-1122.

McCormick DP. Herpes-simplex virus as a cause of bell’s palsy. Lancet 1972; 1:937-939.

McGovern FH, Hansel JS. Decompression of the facial nerve in experimental Bell’s palsy. Laryngoscope 1955; 71:1090.

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References

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46:743-747.

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