Bell’s Palsy

Diagnostic and Treatment Considerations

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
(www.explosm.net)

All images obtained via Google

search unless otherwise specified.
All images used without
permission.
 Outline
 Anatomy
 Pathophysiology
 Diagnostics
 Treatment
 Conclusions

Before Bell’s Palsy After Bell’s Palsy

 Facial Nerve
Anatomy

 Contains 7,000-10,000 fibers

 Nuclei
 Somatic – Motor
 Taste – Tractus solitarius
 Secretomotor – Superior salivatory
 Segments
 Intracranial (cisternal)
 Meatal
 Labyrinthine
 Tympanic
 Mastoid (J Neurol Neurosurg Psychiatry 2001;71:149-154)

 Extratemporal
 Facial Nerve
Segments

 Intracranial
 Meatal
 Labyrinthine
 Tympanic
 Mastoid
 Extratemporal

(www.entusa.com)
 Facial Nerve
Segments

 Intracranial
 Meatal
 Labyrinthine
 Tympanic
 Mastoid
 Extratemporal

(radiopaedia.org) (info.med.yale.edu)
 Facial Nerve
Segments

 Intracranial
 Meatal
 Labyrinthine
 Tympanic
 Mastoid

(Lalwani AK, ed. Current Diagnosis and Treatment:

Otolaryngology Head and Neck Surgery, 2nd Ed.)
 Extratemporal

 Internal auditory canal (IAC)

 8mm
 Zero branches
 Facial Nerve
Segments

 Intracranial
 Meatal
 Labyrinthine
 Tympanic
 Mastoid

(Lalwani AK, ed. Current Diagnosis and Treatment:

Otolaryngology Head and Neck Surgery, 2nd Ed.)
 Extratemporal

 IAC to geniculate ganglion

 3-4mm
 Three branches from geniculate ganglion
 Facial Nerve
Segments

 Intracranial
 Meatal
 Labyrinthine
 Tympanic
 Mastoid

(Lalwani AK, ed. Current Diagnosis and Treatment:

Otolaryngology Head and Neck Surgery, 2nd Ed.)
 Extratemporal

 Geniculate ganglion to pyramidal eminence

 8-11mm
 Zero branches
 Facial Nerve
Segments

 Intracranial
 Meatal
 Labyrinthine
 Tympanic
 Mastoid
 Extratemporal

 Pyramidal eminence to stylomastoid foramen

 8-14mm
 Three branches
 Facial Nerve
Segments

 Intracranial
 Meatal
 Labyrinthine
 Tympanic
 Mastoid
 Extratemporal

 Stylomastoid foramen to major branches (www.facialparalysisinstitute.com)

 15-20mm
 House-Brackmann Scale
(House 1985)

Grade Appearance Forehead Eye Mouth

I normal normal normal normal

slight weakness moderate to good complete closure

II normal resting tone movement minimal effort
slight asymmetry

non-disfiguring weakness slight to moderate complete closure slight weakness

III normal resting tone movement maximal effort maximal effort

disfiguring weakness asymmetric with

IV normal resting tone
none incomplete closure
maximal effort

minimal movement
V asymmetric resting tone
none incomplete closure slight movement

VI asymmetric none none none

 House-Brackmann Scale
(House 1985)

Grade Appearance Forehead Eye Mouth

I normal normal normal normal

slight weakness moderate to good complete closure

II normal resting tone movement minimal effort
slight asymmetry

non-disfiguring weakness slight to moderate complete closure slight weakness

III normal resting tone movement maximal effort maximal effort

disfiguring weakness asymmetric with

IV normal resting tone
none incomplete closure
maximal effort

minimal movement
V asymmetric resting tone
none incomplete closure slight movement

VI asymmetric none none none

 House-Brackmann Scale
(House 1985)

Grade Appearance Forehead Eye Mouth

I normal normal normal normal

slight weakness moderate to good complete closure

II normal resting tone movement minimal effort
slight asymmetry

non-disfiguring weakness slight to moderate complete closure slight weakness

III normal resting tone movement maximal effort maximal effort

disfiguring weakness asymmetric with

IV normal resting tone
none incomplete closure
maximal effort

minimal movement
V asymmetric resting tone
none incomplete closure slight movement

VI asymmetric none none none

 House-Brackmann Scale
(House 1985)

Grade Appearance Forehead Eye Mouth

I normal normal normal normal

slight weakness moderate to good complete closure

II normal resting tone movement minimal effort
slight asymmetry

non-disfiguring weakness slight to moderate complete closure slight weakness

III normal resting tone movement maximal effort maximal effort

disfiguring weakness asymmetric with

IV normal resting tone
none incomplete closure
maximal effort

minimal movement
V asymmetric resting tone
none incomplete closure slight movement

VI asymmetric none none none

 House-Brackmann Scale
(House 1985)

Grade Appearance Forehead Synkinesis

Eye Mouth

I normal normal normal

normal normal

slight weakness moderate to good

synkinesis
complete
barely
closure
noticeable
II normal resting tone movement contractureminimal
or spasm
slight asymmetry
effort absent

non-disfiguring weakness slight to moderate

obvious but
complete
not disfiguring
closuresynkinesis
slight weakness
III normal resting tone movementmass movement
maximalor effort
spasm present
maximal effort

disfiguring weakness asymmetric with

IV normal resting tone
severe
none synkinesis,
incomplete
mass movement,
closure or spasm
maximal effort

minimal movement
V asymmetric resting tone
synkinesis,
none contracture,
incomplete
andclosure
spasm usually
slight absent
movement

VI asymmetric noneno synkinesis, contracture,

none or spasmnone
 House-Brackmann Scale
(House 1985)

Grade Appearance Synkinesis

I normal normal

slight weakness synkinesis barely noticeable

II normal resting tone contracture or spasm absent

non-disfiguring weakness obvious but not disfiguring synkinesis

III normal resting tone mass movement or spasm present

disfiguring weakness
IV normal resting tone
severe synkinesis, mass movement, or spasm

minimal movement
V asymmetric resting tone
synkinesis, contracture, and spasm usually absent

VI asymmetric no synkinesis, contracture, or spasm

 Bell’s Palsy
 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

(BMJ 2004; 329(7465):553–557.)

 Bell’s Palsy
Demographics

 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
Natural History

 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

 Outcomes of 1011 untreated patients (Peiterson 1982)

 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

 Bell’s Palsy
Natural History

 Outcomes of 1011 untreated patients (Peiterson 1982)

 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
 Bell’s Palsy
Associated Symptomatology

 Outcomes of 1011 untreated patients (Peiterson 1982)

 Reduced stapedial reflex
 Postauricular pain
 Dysgeusia
 Decreased lacrimation
 Phonophobia
 Bell’s Palsy
Pathophysiology

 Historically thought to be idiopathic

 Two theories
 Vascular congestion
 Viral polycranioneuropathy
 Pathophysiology
Vascular Congestion

 Autonomic vascular instability (Mcgovern 1955)

 Spasm of nutrient arterioles
 Secondary ischemia
 Nerve edema
 Compression within
fallopian canal
 Possible triggers
 Cold temperature
 Psychosomatic
 Pathophysiology
Infectious

 Acute infectious polyneuritis cerebralis

acusticofacialis by Antoni in 1919
(Freidman 2000)

 Facial nerve edema from viral

inflammatory response
 HSV proposed etiology in 1972 (McCormick)

(www.facialnervecenter.org)
 Pathophysiology
Infectious

 Burgess (1994)
 Surgita (1995)
 Murakami (1996)
 Furuta (1998)
 Pathophysiology
Infectious

 Burgess (1994)  Patient who died six days after

developing Bell’s palsy
 Surgita (1995)
 HSV type 1 (HSV-1) DNA in temporal
 Murakami (1996) bone section
 Furuta (1998)
 Pathophysiology
Infectious

 Burgess (1994)  Inoculation of mice with HSV-1 DNA

 Auricle in 104
 Surgita (1995)
 Tongue in 30
 Murakami (1996)  Transient facial paresis
 Furuta (1998)  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
 Pathophysiology
Infectious

 Burgess (1994)  Transmastoid decompression during

active phase of disease
 Surgita (1995)
 HSV-1 in endoneural fluid of 11 out of 14
 Murakami (1996) with Bell’s palsy
 Furuta (1998)  No varicella-zoster virus (VZV)
 No Epstein Barr
 Ramsay Hunt
 VZV present
 No HSV-1
 Trauma or neoplasm
 No HSV-1
 No VZV
 Pathophysiology
Infectious

 Burgess (1994)  Polymerase chain reaction of saliva

 Bell’s palsy in 47
 Surgita (1995)
 Ramsay Hunt in 24
 Murakami (1996)  Healthy, HSV-positive in 16 (control)
 Furuta (1998)  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
 Pathophysiology
Histolopathology

 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 (Lalwani AK, ed. Current Diagnosis and Treatment:
Otolaryngology Head and Neck Surgery, 2nd Ed.)
 Neurotmesis
 Bell’s Palsy
Diagnostics

 History
 Physical examination
 Radiology
 Topography
 Audiology
 Electrophysiology
 Diagnostics
History and Physical Examination

 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

 Hearing loss or vertigo  Symmetric audiological function

 Absent ipsilateral acoustic reflex
 Timing  Bell’s palsy questioned if vertiginous
 Sudden onset  Clinical threshold for cerebrovascular
 Evolution over 2-3 weeks accident

 Presence of ear disease

 Vesicular eruption
 Bilateral
 Recurrence
 Diagnostics
History and Physical Examination

 Hearing loss or vertigo

 Timing  Occurs over 24-48 hours
 Can progress to complete paralysis
 Sudden onset over 1-7 days
 Evolution over 2-3 weeks  Rule out neoplasm if evolution past
3 weeks
 Presence of ear disease
 Vesicular eruption
 Bilateral
 Recurrence
 Diagnostics
History and Physical Examination

 Hearing loss or vertigo

 Timing
 Sudden onset
 Evolution over 2-3 weeks
 Presence of ear disease  Chronic otitis media
 Cholesteatoma
 Vesicular eruption
 Bilateral
 Recurrence
 Diagnostics
History and Physical Examination

 Hearing loss or vertigo

 Timing
 Sudden onset
 Evolution over 2-3 weeks
 Presence of ear disease
 Vesicular eruption  Ramsay-Hunt syndrome

 Bilateral
 Recurrence
 Diagnostics
History and Physical Examination

 Hearing loss or vertigo

 Timing
 Sudden onset
 Evolution over 2-3 weeks
 Presence of ear disease
 Vesicular eruption
(ent.uci.edu)
 Bilateral  Guillain-Barre syndrome
 Lyme disease
 Recurrence  Intracranial neoplasm
 Diagnostics
History and Physical Examination

Hearing loss or vertigo

(Rev Bras Otorrinolaringol 2002; 68(5):755-760)



 Timing
 Sudden onset
 Evolution over 2-3 weeks
 Presence of ear disease
 Vesicular eruption
 Bilateral
 Recurrence  Usually excludes Bell’s palsy
 Melkersson-Rosenthal syndrome
 Diagnostics
Radiology

 Localize lesion
 Computed tomography
 Trauma
 Mastoiditis
 Cholesteatoma
 Magnetic resonance imaging (MRI)
 Nerve enhancement
 No correlation with site or degree of enhancement
 Exclude neoplasm
 Diagnostics
Topography

 Schirmer test → greater superficial petrosal

 Stapedial reflex → stapedial branch
 Electrogustometry → chorda tympani
 Salivary flow → chorda tympani
 Unable to predict location or outcome
 Diagnostics
Audiology

 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
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)
 Diagnostics
Electrophysiology

 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
 Diagnostics
Electrophysiology

 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
 Diagnostics
Electrophysiology

 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  NET, MST, and ENoG normal
 Axonotmesis  No voluntary motor action potentials on EMG

 Neurotmesis
 Diagnostics
Electrophysiology

 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  NET, MST, and ENoG with rapid and complete
degeneration
 Neurotmesis  EMG
 No voluntary motor action potentials
 Myogenic fibrillation potentials after 10-14 days
 Diagnostics
Electrophysiology

 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  Similar results as axonotmesis
 Less predictable outcome
 Cannot differentiate between the two
 Electrophysiology
Nerve Excitability Test

 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
Maximum Stimulation 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
Electroneuronography

 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
(Am J Otol 1992; 13:127–133.)
 Electrophysiology
Electroneuronography

 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
Electromyography

 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
 Treatment
 Observation
 Monitor progression
 Eye care
 Medical
 Steroids
 Antivirals
 Surgical
decompression

(www.vgcats.com)
 Treatment
Steroids Beneficial

 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 Not 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
Antivirals

 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
Surgical

(Brackmann 2010)
 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

(Brackmann 2010)
 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 (Gantz 1999)

(Brackmann 2010)
 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
Algorithm

(Brackmann 2010)
 Conclusion
 Most common diagnosis of facial paralysis
 Diagnosis of exclusion
 Prognostic information with electrophysiology
 Medical therapy
 Steroids
 Antivirals
 Surgical
decompression
 ENoG with (www.explosm.net)
>90% degeneration
 No voluntary EMG activity within 14 days of paralysis
 References
Adour KK, Ruboyianes JM, Von Doersten PG, et al. Bell’s palsy treatment with acyclovir and prednisone compared with
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.
Axelsson S, Lindberg S, Stjernquist-Desatnik A. Outcome of treatment with valacyclovir and prednisone in patients with Bell’s
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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