B7.024 Bell's Palsy Flashcards
corticobulbar tract
supplies all UMN innervation to the cranial nerves
upper face innervation
bilateral
both hemispheres
lower face innervation
contralateral hemisphere
central facial weakness
only lower facial weakness
UMN type lesion (bc upper face still receives innervation from ipsilateral brain)
peripheral facial weakness
entire hemisphere is weak (upper and lower face)
LMN type lesion
where would a peripheral facial weakness lesion localize
between brainstem and muscles
2 classes of peripheral facial weakness lesions
intra-axial = inside brainstem extra-axial = outside brainstem
hallmark of a brainstem lesion
“alternating hemiplegia”
if nuclei within the brainstem are damaged, the corticospinal system which also runs through the brainstem would be damaged as well
would see body weakness on the opposite side of facial weakness
pattern of deficits for brainstem lesions
ipsilateral CN
contralateral long tracts (weakness, numbness)
how to rule out intra-axial lesions
no long tract symptoms / signs
where does the facial nerve exit the brainstem
pons
4 nuclei of the facial nerve
facial motor nucleus
gustatory nucleus
main sensory nucleus
superior salivatory nucleus
functions of the facial nerve
facial muscle movement
taste on anterior 2/3 of tongue
ear region sensation
parasympathetic salivation / lacrimation
facial motor nucleus innervation
face muscles
stapedius
digastric
gustatory nucleus innervation
taste on anterior 2/3 of tongue
main sensory nucleus innervation
ear region sensation
superior salivatory nucleus innervation
lacrimal, submandibular, sublingual glands
patterns of facial nerve deficits
facial weakness
hyperacusis
decreased taste
dry eyes
why is it important to understand the basic course of the facial nerve
branch points help to localize the site of the lesions
geniculate ganglion
contains nerve cell bodies of all sensory nerve branches of the facial nerve
important of a lesion located after the stylomastoid foramen
increases likelihood of a malignant parotid tumor
higher up lesions are usually benign
list the relevant branch points of facial nerve proximally to distally
geniculate ganglion
- greater petrosal nerve to pterygopalatine ganglion (lacrimal gland)
- nerve to stapedius (hearing)
- chorda tympani (taste, salivatory glands)
- *stylomastoid foramen**
- facial motor branches
how is taste sensation tested
table salt and table sugar
what might you see on an MRI in bell’s palsy
increased signal intensity in the internal auditory canal
nerve / blood barrier broken down
what is Bell’s palsy
idiopathic
peripheral CN 7 palsy
Bell’s palsy pathology
based on autopsy specimens and clinical observations at surgery (doesn't kill people) intraneural inflammation (+/- segmental demyelination) swelling and compression within the Fallopian canal and the perineurium (+/- axon loss)
suspected relationship between HSV1 and Bell’s palsy
can be isolated from nasopharynx of people with Bell’s
HSV antibody titer rises
virus isolated from epineurium of biopsy specimen
PCR positive for HSV in endoneurial fluid of Bell’s patients
saliva positive for HSV by PCR in 11/38 Bell’s patients and 0/10 normal controls
components of natural history of Bell’s palsy
proportion complete recovery time to recovery complications -aberrant re-innervation -hemi-facial spasm
outcomes by which degree of recovery from Bell’s palsy is measured
primary motor function -symmetry at rest -forehead -eye closure -mouth secondary defects -synkinesis -gustatory tears -facial spasm
synkinesis
aberrant reinnervation
due to Wallerian degeneration in some axons leading to nerve regeneration
if connective tissue is damaged, nerve can regenerate to the wrong place
examples of synkinesis
people wink when they try to smile
tear up when smiling
house and brackmann grading scale
1 = normal
6 = total paralysis
lower number is better in recovery from Bell’s
what % of patients recover well from Bell’s
85% have grades of 1-2 on house and brackmann scale
15% do poorly (grades 3-6)
time to recover form Bell’s
initiation of recovery -within 3 weeks (85%) -after 8 weeks (10%) medial time to final recovery -45 to 60 days
poor prognostic factors in Bell’s
older age non ear region pain complete palsy gradual onset vertigo diabetes HTN
why is vertigo indicative of poor prognosis
CN 8 (vertigo) is next to CN 7 (Bell’s) and thus damage to CN 8 may signify more severe inflammation
components of treatment of Bell’s
prevention of exposure keratitis
medications
facial nerve decompression
why is a patient with bell’s at increased risk of exposure keratitis
decreased eye closure
decreased lacrimal gland function
what reduces the risk of bell’s (aka why isn’t it very common to begin with)
preservation of corneal sensation
basically, people can feel their eye getting irritated and take action against it
preventive interventions for exposure keratitis
eye lubrication
eye patching
mainstay of therapy for Bell’s
steroids
- reduce inflammation
- reduce compression within temporal bone
other treatments for Bell’s
acyclovir
-treat underlying infection
surgery
-relieve compression by fallopian canal and perineurium
steroid regimens for Bell’s
prednisolone 60 mg daily x 5, taper by 10 (total 10 days)
OR
prednisolone 25 mg BID x 10 days
how well do steroids work in bells
highly likely to be effective in increasing the likelihood of good facial functional recovery by about 12 %
antiviral recommendation in Bell’s
may be offered to patients with new onset Bells
should be counseled that a benefit from antivirals has not been established and if there is a benefit it is likely that it is at best modest
other therapies for Bell’s that lack evidence for support
facial nerve re-education
Kabat physical rehab
cutaneous electrical stimulation
acupuncture
